I have read what appear to me to be conflicting study results so I wanted to get other people's thoughts about this so I know whether to stay with my statin dosage, lower it or increase it. FYI - I have coronary artery disease 30% plaque in a few spots (I'm 52 and exercise a lot) My biological father had the same issue. Ive always eaten healthy. I also have prostate cancer that psma/pet indicates as metastatic. PSA was 38 before starting on Lupron intermittent Lupron.
I'm adding a couple links here. If you have time, please read and then tell me what you think is best to fight off the cancer without totally abandoning the statins. I did read years ago that a 2.5 mg dose of Crestor reduced total cholesterol by 32%, 20 mg dose by 41% and 40mg by 48%. Thus, if reducing cholesterol (assuming the bad particles in this figure are similar %) is good for reducing plaque buildup and increasing longevity / avoidance of a heart attack, then I can go as low as 2.5mg by cutting my Crestor pills. However, it appears from a couple studies that increase statin doses help fight metastatic prostate cancer. If that is truly the case then what's with this other article I read this weekend saying that high cholesterol helps reduce prostate cancer? Maybe it one of those things were one thing is better to prevent cancer but once you have cancer then going in the opposite direction is better? Hmm, that's why I wanted to see if someone smarter than me can explain or hypothesize this so I can decide what to do with the statin use.
This statement from one of the links probably answers my question: However, being diagnosed with high cholesterol usually lead to treatment, often with statins. So the researchers think the statin treatment might explain the protective effect, rather than high cholesterol itself. They adjusted for other risk factors, such as age, gender, ethnicity, and other common causes of death. Having a diagnosis of high cholesterol was linked to a: 22% lower risk of death in lung cancer 43% lower risk of death in breast cancer 47% lower risk of death in prostate cancer.
The data on statins and prostate cancer is all over the place. Some studies say some effect, some say no effect. Here's an example of each (there are MANY more where these came from:
The problem with all such studies is that there has never been a prospective clinical trial where patients are randomized to statin or placebo. That is the only kind of trial that would answer the question of whether it helps or not. (Data on aspirin and metformin are similarly ambiguous).
Lacking a clear answer, I think you should do whatever your cardiologist recommends.
Solid tumors accumulate cholesterol. PCa tumors that accumulate the most amounts of cholesterol are more aggressive. Resistance to ADT can involve the generation of androgen from cholesterol in PCa cells. And if PCa cells can't get the cholesterol they want, they can synthesize it. Thus, it makes sense to use a statin if on ADT.
Does it make sense to start using a statin following a PCa diagnosis? Could cholesterol be protective at an ealy stage?
[1] In a recent French study of radical prostatectomy [RP] patients:
"low HDL-cholesterol level was associated with locally advanced PCa" (60% increased risk).
[2] In a 2017 German study of RP patients:
"We found that patients with HCE {hypercholesterolemia} had a significantly higher incidence of poorly differentiated PC (Gleason score ≥7b, 81.1% vs. 4.9%), advanced local tumor stage (≥pT3, 57.7% vs. 22.2%), and nodal involvement (19.8% vs. 1.6%).
"Multivariate logistic regression analysis identified hypercholesterolemia as a risk factor for aggressive and/or advanced PC (OR 2.01, p<0.001) whereas statin intake showed an odds ratio of 0.49 ... indicating a negative association with high-risk PC."
[3] However, in a 2016 Japanese study:
"Low preoperative serum TC {total cholesterol} levels were associated with an increased risk of BCR {biochemical recurrence} among prostate cancer patients who underwent RP."
This study cites [4] as offering a possible explanation.
[4] (2012 - U.S.:
"The concept of the “U shaped curve” refers to the higher levels of mortality found on either end of the cholesterol level spectrum that many investigators discovered when studies were performed to assess the potential relationship between circulating cholesterol and mortality."
An "important reason for higher mortality at the low end of the U arises from the cholesterol-lowering effect of cancer itself; therefore, the low end of the curve likely includes an excess of subjects with pre-existing cancer."
...
I'm going to stick with the view that one should be offered a high-dose statin after a PCa diagnosis - regardless of lipid numbers.
good info pjo, I have always had HDL between 27-34 and Ive always ate healthy and exercised. I just cant raise my HDL. I'd fall into that 60% increased risk category. I'll stick with the 20 mg of crestor for now. I can always increase the mg later if told to.
As a matter of interest, what are your triglycerides [Tri] generally at? The Tri:HDL-C ratio is considered to be a good surrogate for insulin resistance, which I consider to be a major PCa problem.
I eat very healthy now. Even when I thought I was a healthy eater previously, my triglycerides were always over 200. For the past two years I've kept them under eighty. I'm still leery about starting zytiga because of the possibility of high blood pressure.
this is a recent, large population study dealing with adding statin and metformin post-diagnosis.
"Conclusions:
CaP mortality was substantially lower in high-risk CaP post-diagnostic users of statin within 6 years of follow-up. A synergistic effect of statin and metformin was observed in patients with M1 disease only. "
But I could have showed just as many studies that suggested a positive effect. There are no definitive data. Lacking that, since low dose aspirin, metformin, and statins are relatively harmless and cheap and may even do some good other than with PC, my opinion is why not?
I spent a little time looking over the reports. The problem with bio-statistics and statistics in general is that they analysis could go wrong in so may ways: parameter mis-specification and selection bias are two main ones. But so is the model selection, and data integrity (and so on).
More specifically, I just picked your first reports below, I have jotted down my two cents.
1. ncbi.nlm.nih.gov/pmc/articl...
This report suffers from selection bias. What it ACTUALLY shows (if all else is true) vs what it CLAIMS to show are two different things.
It starts off by 12052 patients, then quickly reduced it to "diabetic"-only patients with 885 members. Of which some are on metformin, some on a statin and some on both.
I think it'd be rational to assume that the metformin users are already the HIGHER risk group. Not only they have double the % of statin users (cardiovasculat issues perhaps), one has to assume that they have a more severe case of diabetes than the other diabetics who do no take metformin.
Next is the stage of the disease. More than 95% of the sample size is T2 or below.
So I'm not prepared to accept the conclusion of the report as stated.
EVEN IF there were no selection bias, the most that the report could've claimed is that:
"among early stage diabetic PCa patients post RP, there's no OS benefits to metformin users."
It's clear that it is mute on post-diagnosis use in non-diabetic patients, and in the more advanced disease.
Again, I think we will encounter similar issues in reports that are both pro and against. We need to dig a little deeper before we assign credence. The researchers are just human, mistake prone, with an incentive to publish.
I made no claims for the reliability of any of those studies - you asked to see some studies so I showed you. I very much agree. ALL the research on metformin, statins and aspirin are retrospective studies with inherent selection bias. The only valid claim the authors can make is that it needs further study. There never has been a prospective randomized trial that would provide proof. That is why I don't deny they MAY have value (although that value, if any, is clearly small, so it would require a very large sample size to be sufficiently powered), but neither do I make any claims for them.
I have no interest in destroying hope or taking away the modicum of control one feels when one makes changes in things he does or uses. I generally don't comment on food and diet studies, which are notoriously biased, and I only comment on supplements if I think they may be harmful. Vitamin E (commercially available) has been proven to be harmful. A few supplements (e.g., pomegranate extract) have been proven to have no effect. A good case can be made for sulforaphane (with certain caveats).
I’m sorry if I came across as criticizing your generously volunteered information. That was not my intent at all. It’s more along what you said: we should all read the reports critically and don’t be swayed by the headlines or titles alone. We all heard about “lies, damned lies, and statistics.”
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